Cytomegalovirus (CMV) is the most frequent known cause of congenital viral infections in humans and is endemic throughout the world. congenitally infected infants may be born with various hematologic, neurologic, and developmental symptoms including hepatosplenomegaly, petechiae, intracranial calcifications, microcephaly, hydrocephalus, hearing impairment, and growth restriction. We have established a nonhuman primate model for human CMV infection by direct intraperitoneal (IP) inoculation of rhesus fetuses with rhesus CMV (rhCMV). Prior studies have shown infected fetuses develop intrauterine growth restriction (IUGR), ventriculomegaly, and microcephaly, all hallmarks of CMV disease in humans. In addition, fetuses exhibited widespread dissemination of rhCMV DNA, as detected by PCR; infected tissues included liver, spleen, thymus, lymph nodes, and brain. The dams of the fetuses with the most severe pathological outcomes were noted with the lowest levels of anamnestic anti-rhCMV IgG immune response. Currently we are examining the role of cytokines in CMV-induced fetal disease and the effect of differing viral titers on fetal outcome. Fetuses (N=10) are directly inoculated IP via ultrasound-guidance with rhCMV during the early second trimester, then monitored sonographically each week (growth, fetal hemodynamics). Blood samples are collected from the fetus and dam every 10 days during gestation until tissue harvest (term) for virus isolation and hematologic and immunologic assessments. Given the strong conservation between rhCMV and human CMV, these studies will be particularly relevant to furthering the understanding, treatment, and prevention of CMV disease in humans. *KEY*Cytomegalovirus, Fetus, Growth, Neuropathology, Pathogenesis